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Athletic heart syndrome is a constellation of structural and functional changes that occur in the heart of people who train for > 1 h most days. The syndrome is asymptomatic; signs include bradycardia, a systolic murmur, and extra heart sounds. ECG abnormalities are common. Diagnosis is clinical or by echocardiography. No treatment is necessary. The syndrome is significant because it must be distinguished from serious cardiac disorders.

Intensive, prolonged endurance and strength training produces many physiologic adaptations. Volume and pressure loads in the left ventricle (LV) increase, which, over time, increase LV muscle mass, wall thickness, and chamber size. Maximal stroke volume and cardiac output increase, contributing to a lower resting heart rate and longer diastolic filling time. Lower heart rate results primarily from increased vagal tone, but decreased sympathetic activation and other nonautonomic factors that decrease intrinsic sinus node activity may play a role. Bradycardia decreases myocardial O₂ demand; at the same time, increases in total Hb and blood volume enhance O₂ transport. Despite these changes, systolic and diastolic function remains normal. Structural changes in women are typically less than those in men of the same age, body size, and training.

Symptoms and Signs

There are no symptoms. Signs vary but may include bradycardia; an LV impulse that is laterally displaced, enlarged, and increased in amplitude; a systolic ejection (flow) murmur at the left lower sternal border; a 3rd heart sound (S₃) due to early, rapid diastolic ventricular filling; a 4th heart sound (S₄), heard best during resting bradycardia because diastolic filling time is increased; and hyperdynamic carotid pulses. These signs reflect structural cardiac changes that are adaptive for intense exercise.

Diagnosis

Findings are typically detected during routine screening or during evaluation of unrelated symptoms. Most athletes do not require extensive testing, although ECG is often warranted. If symptoms suggest a cardiac disorder, ECG, echocardiography, and exercise stress testing are done.

Athletic heart syndrome is a diagnosis of exclusion; it must be distinguished from disorders that cause similar findings but are life threatening (eg, hypertrophic or dilated cardiomyopathies, ischemic heart disease, arrhythmogenic right ventricular dysplasia).

ECG typically shows sinus bradycardia; rarely, heart rate is < 40 beats/min. Sinus arrhythmia often accompanies the slow heart rate. Resting bradycardia may predispose to increased atrial or ventricular ectopy, including wandering supraventricular pacemaker and, uncommonly, atrial fibrillation, but pauses after ectopic beats do not exceed 4 sec. First-degree atrioventricular (AV) block is detected in up to ¹⁄₃ of athletes; 2nd-degree AV block (mainly type 1) that occurs during rest but disappears with exercise is less common. Third-degree AV block is abnormal and should be investigated thoroughly. Waveform changes include high voltage QRS complexes with inferolateral T-wave changes or strain pattern, which reflect LV hypertrophy, and early depolarization changes with biphasic T waves in anterior leads, which reflect inhomogeneous repolarization from reduced resting sympathetic tone. Both resolve with exercise. Deep anterolateral T-wave inversion and incomplete right bundle branch block may also occur. ECG changes correlate poorly with level of training and cardiovascular performance.

Echocardiography can distinguish athletic heart syndrome from cardiomyopathies (see Table 2: Sports and the Heart: Features Distinguishing Athletic Heart Syndrome From Cardiomyopathy), but because there is a continuum from physiologic to pathologic cardiac enlargement, the distinction is not always clear. In general, echocardiographic changes correlate poorly with level of training and cardiovascular performance. Trace mitral regurgitation and tricuspid regurgitation are commonly detected.

Table 2
Features Distinguishing Athletic Heart Syndrome From Cardiomyopathy Feature Athletic Heart Syndrome Cardiomyopathy Left ventricular hypertrophy* < 13 mm > 15 mm Left ventricular end-diastolic diameter† < 60 mm > 70 mm Diastolic function Normal (E:A ratio > 1) Abnormal (E:A ratio < 1) Septal hypertrophy Symmetric Asymmetric (in hypertrophic cardiomyopathy) Family history None May be present BP response to exercise Normal Normal or reduced systolic BP response Deconditioning Left ventricular hypertrophy regression No left ventricular hypertrophy regression *A value of 13 to 15 mm is indeterminate. †A value of 60 to 70 mm is indeterminate. E:A ratio = ratio of early to late atrial transmitral flow velocity.

During exercise stress testing, heart rate remains lower than normal at submaximal stress and increases appropriately and comparably to nonathletes at maximal stress; it rapidly recovers after exercise. BP response is normal: Systolic BP increases, diastolic BP falls, and mean BP stays relatively constant. Many resting ECG changes decrease or disappear during exercise; this finding is unique to athletic heart syndrome, distinguishing it from pathologic conditions. However, pseudonormalization of T-wave inversions could reflect myocardial ischemia and thus warrants further investigation in older athletes.

Prognosis and Treatment

Although gross structural changes resemble those in some cardiac disorders, no adverse effects are apparent. In most cases, structural changes and bradycardia regress with detraining, although up to 20% of elite athletes have residual chamber enlargement, raising questions, in the absence of long-term data, about whether the athletic heart syndrome is truly benign.

No treatment is required, although 3 mo of deconditioning may be needed to monitor LV regression as a way of distinguishing this syndrome from cardiomyopathy. Such deconditioning can greatly interfere with an athlete's life and may meet with resistance.

Last full review/revision November 2005

Content last modified November 2005